Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, NY 14214, USA.
J Neurophysiol. 2012 Jul;108(1):200-14. doi: 10.1152/jn.00946.2011. Epub 2012 Apr 11.
A high dose of sodium salicylate temporarily induces tinnitus, mild hearing loss, and possibly hyperacusis in humans and other animals. Salicylate has well-established effects on cochlear function, primarily resulting in the moderate reduction of auditory input to the brain. Despite decreased peripheral sensitivity and output, salicylate induces a paradoxical enhancement of the sound-evoked field potential at the level of the primary auditory cortex (A1). Previous electrophysiologic studies have begun to characterize changes in thalamorecipient layers of A1; however, A1 is a complex neural circuit with recurrent intracortical connections. To describe the effects of acute systemic salicylate treatment on both thalamic and intracortical sound-driven activity across layers of A1, we applied current-source density (CSD) analysis to field potentials sampled across cortical layers in the anesthetized rat. CSD maps were normally characterized by a large, short-latency, monosynaptic, thalamically driven sink in granular layers followed by a lower amplitude, longer latency, polysynaptic, intracortically driven sink in supragranular layers. Following systemic administration of salicylate, there was a near doubling of both granular and supragranular sink amplitudes at higher sound levels. The supragranular sink amplitude input/output function changed from becoming asymptotic at approximately 50 dB to sharply nonasymptotic, often dominating the granular sink amplitude at higher sound levels. The supragranular sink also exhibited a significant decrease in peak latency, reflecting an acceleration of intracortical processing of the sound-evoked response. Additionally, multiunit (MU) activity was altered by salicylate; the normally onset/sustained MU response type was transformed into a primarily onset response type in granular and infragranular layers. The results from CSD analysis indicate that salicylate significantly enhances sound-driven response via intracortical circuits.
高剂量的水杨酸钠会在人类和其他动物中暂时引起耳鸣、轻度听力损失，甚至可能引起听觉过敏。水杨酸盐对耳蜗功能有明确的影响，主要导致听觉输入到大脑的适度减少。尽管外周敏感性和输出降低，水杨酸盐仍会在初级听觉皮层（A1）水平引起声音诱发场电位的反常增强。先前的电生理研究已经开始描述 A1 中丘脑接受层的变化；然而，A1 是一个具有皮质内回传连接的复杂神经网络。为了描述急性系统性水杨酸盐处理对 A1 各层的丘脑和皮质内声音驱动活动的影响，我们在麻醉大鼠中应用电流源密度（CSD）分析来采样皮质各层的场电位。CSD 图谱通常以大潜伏期、单突触、丘脑驱动的在颗粒层的汇流为特征，随后是较小幅度、较长潜伏期、皮质内驱动的在颗粒上层的汇流。在系统性给予水杨酸盐后，在较高的声音水平下，颗粒层和颗粒上层的汇流幅度几乎增加了一倍。颗粒上层汇流幅度的输入/输出函数从约 50dB 处的渐近变为急剧非渐近，通常在较高的声音水平下主导颗粒层汇流幅度。颗粒上层汇流也表现出明显的峰值潜伏期缩短，反映了声音诱发反应的皮质内处理加速。此外，水杨酸盐改变了多单位（MU）活动；通常的起始/维持 MU 反应类型在颗粒层和下颗粒层中转变为主要起始反应类型。CSD 分析的结果表明，水杨酸盐通过皮质内回路显著增强了声音驱动的反应。
